Interactions between different media and follicle‐stimulating hormone supplementation on in vitro culture of preantral follicles enclosed in ovarian tissue derived from collared peccaries (Pecari tajacu Linneaus, 1758)

The aim was to verify the effect of follicle‐stimulating hormone (FSH) supplementation to α‐MEM+ or TCM199+ media on the in vitro development of ovarian preantral follicles (PFs) derived from collared peccaries. Ovaries (n = 5 pairs) were collected and divided into fragments destined to control group (non‐cultured) or treatments that were cultured for 7 days. The PFs morphology, growth and activation were evaluated by classical histology. The immunohistochemistry markers Ag‐NOR and PCNA were used for nuclear proliferation analysis, and the picrosirius red labelling was used for ovarian extracellular matrix (ECM) evaluation. After 7‐day culture, only the TCM199+ treatment maintained the proportion of intact PFs similar to day 1 (63.2%), but no differences were found among treatments (p > .05). In addition, a significant increase in the growing follicles proportion was verified for all the treatments, indicating follicular activation (p > .05). By the Ag‐NOR analysis, only the TCM199+/FSH maintained the nuclear proliferation similar to the first day (p > .05). The picrosirius red staining revealed that the ECM remained intact in all the treatments (p > .05). We suggest the use of TCM199+ medium supplemented of FSH for the in vitro development of peccaries PFs under 7‐day culturing conditions.     

Induction of diplodiosis, a neuromycotoxicosis, in domestic ruminants with cultures of indigenous and exotic isolates of Diplodia maydis

Diplodiosis, a neuromycotoxicosis, principally of cattle, which is characterized by ataxia, paresis and paralysis, was induced in 13 cattle, 16 sheep and 3 goats, by dosing them with Diplodia maydis [= D. zeae (Schw.) Lév.] cultured on sterilized maize seeds. The results of these experiments confirmed the findings of earlier workers that diplodiosis is a mycotoxicosis caused by D. maydis. The intoxication was induced with cultures of South African isolates of D. maydis obtained from local maize, one of which was associated with a suspected field outbreak, and with cultures of isolates from maize imported from the United States of America and Argentina. Other findings emerging from the experiments were, inter alia, that cultures incubated for less than 8 weeks were seemingly non-toxic, that there was little individual variation in response of cattle to cultures of the different toxic isolates or batches of the isolates, that apparent relapses of clinical signs can occur several weeks after dosing had ceased and that a small percentage of animals can show permanent locomotory disturbance. Light microscopical examination revealed no lesions in acutely affected animals, but an extensive laminar subcortical status spongiosis was evident in the cerebrum and cerebellum of a sheep that had been long paralysed and a steer that had permanent locomotory disturbance.     

Leukoencephalomalacia in two horses induced by oral dosing of fumonisin B1

Leukoencephalomalacia (LEM) was induced by the oral administration of fumonisin B1 (FB1) to 2 horses: a filly received 59.5 mg/kg of a 50% preparation of FB1, administered in 21 doses of 1.25-4 mg/kg over 33 days; a colt, 44.3 mg/kg of 95% pure FB1 in 20 doses of 1-4 mg/kg in 29 days. Both animals developed nervous signs such as apathy, changes in temperament, inco-ordination, walking into objects, and one showed paralysis of the lips and tongue. Characteristic lesions of LEM were present in the brains. These trials proved conclusively that FB1 can induce LEM in horses.     

Blindness and encephalopathy caused by Helichrysum argyrosphaerum DC. (Compositae) in sheep and cattle.

An outbreak of amaurosis and paresis was observed amongst sheep, and occasionally cattle, which had been grazing on pastures consisting mainly of Helichrysum argyrosphaerum DC. A similar syndrome was produced by feeding the suspect plant to sheep, thereby providing proof if its toxicity. Although none of the sheep became blind and only one developed paralysis, typical sponly lesions were detected in the brains and optic fasciculi of all the experimental animals. The lesion had specific predilection sites, such as the white matter around the lateral ventricles, the optic tracts plus chiasm, the pyramidal tracts and the brachium pontis. Enlargement of the optic fasciculi furthermore gave rise to malacia, papilloedema and retinal changes. Some aged sheep developed cataracts approximately 2-3 months after the initial outbreaks of amaurosis had occurred. Circumstantial and histopathological evidence suggests that the cataracts may be due to chronic Helichrysum poisoning, but this could not confirmed in the present investigation.     

Leukoencephalomalacia in a horse induced by fumonisin B1 isolated from Fusarium moniliforme

Each of two horses was dosed by stomach tube with culture material on maize of Fusarium moniliforme MRC 826. One horse developed severe hepatosis and mild oedema of the brain after 6 doses of 2.5 g of culture material/kg body mass/day in 7 days. The second horse, in a similar experiment but at a dosage rate of 1.25 g/kg/day, developed mild hepatosis and moderate oedema of the brain. In both animals the brain oedema was particularly noticeable in the medulla oblongata. The mycotoxin fumonisin B1 was extracted and purified from the culture material of F. moniliforme MRC, 826 which contained approximately 1 g/kg of this compound. A horse was injected intravenously 7 times from Day 0-Day 9 with 0.125 mg of fumonisin B1/kg body mass/day. Clinical signs of neurotoxicosis, which appeared on Day 8, included nervousness followed by apathy, a wide-based stance, trembling, ataxia, reluctance to move, paresis of the lower lip and tongue, and an inability to eat or drink. Euthanasia was performed on the horse on Day 10 while the animal was in a tetanic convulsion. The principal lesions were severe oedema of the brain and early, bilaterally symmetrical, focal necrosis in the medulla oblongata. This report provides experimental evidence that fumonisin B1, produced by F. moniliforme, causes equine leukoencephalomalacia.     

Cardiac glycoside poisoning in sheep caused by Urginea physodes (Jacq.) Bak. and the isolated physodine A

Urginea physodes (Jacq.) Bak., a species closely related to or possibly synonymous with U. pusilla, is described and its distribution given. Four bufadienolides were isolated from U. physodes and the approximated LD50 and cumulative effect of some of them determined in guinea pigs. The most toxic one proved to be mildly cumulative. Typical signs of acute cardiac glycoside poisoning, involving the locomotory, gastro-intestinal, respiratory and cardiac system, were seen in the field cases and/or were experimentally induced by the plant. Similar signs could also be induced by injecting the isolated bufadienolide, physodine A, to a sheep.     

Carbendazim,at concentrations used on pasture for facial eczema control,reduces development of Trichostrongylus colubriformis when sprayed onto infected sheep faeces

Abstract

AIM: To determine whether the fungicide, carbendazim, as applied to pastures for controlling facial eczema (FE), would inhibit development of the free-living stages of the gastrointestinal nematode parasite Trichostrongylus colubriformis.

METHODS: Two studies were conducted, using sheep faeces containing eggs of T. colubriformis. In the first, the faeces were either exposed or not to an application of carbendazim sprayed at the recommended rate for FE control. After spraying, dishes containing the faeces were incubated at 20°C for 14 days, and the resulting third-stage infective larvae (L3) extracted by baermannisation and counted. In addition, naturally infested pasture was also sprayed, and the number of L3 present 7 days later was assessed by cutting herbage samples and extracting larvae by soaking in water and baermannisation. In the second, the faeces were incubated at 20°C for 0, 3 or 7 days before being exposed to no, one or two applications of carbendazim. After further incubation for 14, 11 or 7 days, L3 were similarly extracted by baermannisation and counted.

RESULTS: In the first study, there was a 74% reduction in the number of T. colubriformis larvae recovered from faeces exposed to carbendazim compared with faeces not exposed, but there was no reduction in the number of L3 recovered from herbage. In the second study, faeces incubated for 0 or 3 days prior to exposure to a single application of carbendazim yielded 98% or 89% fewer larvae, respectively, than faeces not exposed. Faeces incubated for 7 days prior to exposure yielded similar numbers of larvae to faeces not exposed.

CONCLUSION: Treatment of pastures with carbendazim for FE control is likely to result in reduced development of the larvae of T. colubriformis, and by inference those of other species, where the application coincides with the presence of freshly deposited faeces containing eggs and developing larvae. However, no effect of treatment on L3 was indicated. The significance of this for on-farm nematode parasite control remains to be determined, as does any potential for strategic applications of carbendazim to pasture aimed at reducing numbers of parasite larvae on pasture. The latter should not be contemplated without due consideration of the implications for the development of anthelmintic resistance.